These investigators proposed to evaluate some of the factors that appear to be important in the development of asthma in children. Some evidence suggests that there is an increased incidence of asthma in children raised in the homes of cigarette smokers. The investigators have postulated that inhalation of mainstream cigarette smoke during pregnancy and or/sidestream smoke by genetically susceptible children increases the incidences of asthma by altering pulmonary immune responses to inhaled antigens through changes in antigen presentation in the lung and or lung-associated lymph nodes. To test this hypothesis, the PIs will evaluate the importance of cigarette smoke exposure as risk factors in the development of Th2 pulmonary immunity and airway hyperreactivity (AHR). Two groups of mice will be exposed to cigarette smoke or clear air in utero, as newborns, and as young adults. The two groups that will be used are; 1) mice on a Balb/c background that are transgenic for the ovalbumin (OVA) T cell receptor (Tg +/-), and 2) nontransgenic Balb/c mice (Tg-/-). Mice will be immunized by inhalation of OVA during air or cigarette smoke exposures, and mice exposed to air or cigarette smoke without OVA will serve as controls. The induction of Th1 and/or Th2 immunity and the development of AHR in exposed and control mice will be determined by; 1) measuring the levels of messenger RNA for IL-2, IL-4, IL-5, IL-12, and IFN-y in cells from the lung and the lung-associated lymph nodes and the production of anti-OVA IgG1, IgG2a, and IgE by these cells; 2) measuring AHR to methacoline; and 3) by evaluating pulmonary histopathology. Roles of lung dendritic cells and lung macrophages will be evaluated as a possible explanation for how cigarette smoke exposures might increase the induction of Th2 immunity to inhaled OVA. The results from these studies could help prevent the development of asthma in susceptible individuals and in the development of future therapeutics for treating asthma.